Myocardial Infarction miocardial infarction by mikeholy


									Myocardial Infarction; Congestive Heart Failure                                         1
Lecture Date 03-03-03                                                                  LJ

                              Myocardial Infarction

 Definition: necrosis of the heart muscle due to interruption of the oxygen supply.
  This interruption may be from:
   Plaque
   Thrombus
   Spasm—most common cause in young, healthy people
   Combination of all Three

 Terminology
   Transmural infarct: more common.
      Ischemic necrosis involves full thickness of ventricular wall.
      Serious and more common
      Can cause rupture or aneurysm
      The wall becomes necrotic and can pouch out and rupture. Rupture =
        immediate death.
   Nontransmural Infarct
      Necrosis limited to inner 1/3 to 1/2 of the ventricular wall.

 Sites of MI:
       Can occur in any area of the heart.
       Most common is left ventricle because it does the most work.

    Severity of MI depends on:
      Which vessel is affected
      Where in the vessel
      Number of vessels involved. Many = more severe MI
      Collateral circulation—new circulation that grows around occlusion. Younger
        patients do not have collateral circulation that is as well developed as older
        people. Collateral circulation takes “a while to develop.”

    Bull’s Eye Theory
      Picture a bull’s eye.
      The center is dead tissue (necrotic). No repair. Dead tissue.
      The next ring is an area of injury. (ischemic) Goal is to try to keep it from
        becoming necrotic. Irritated, red, etc.“Extended MI” means ischemic area
        became necrotic.
      The third ring is an area of swelling. Edema of heart muscle.

    Three Systems of the Heart:
      Electrical conduction system
      Blood supply
      Pumping

 Diagnosis of MI
Myocardial Infarction; Congestive Heart Failure                                          2
Lecture Date 03-03-03                                                                   LJ
    CPK: Creatinine Phosphokinase: Released from dead muscle.
      Starts going up 6-8 hours after damage, peaks in 12-18 hours. Returns to
       normal 3-4 days.
      Goes up with any muscle damage.
      Use as a broad idea of how large the infarct is. (Generally, the higher the
       CPK, the larger the infarct) = more muscle damage.
      Usually see an order: CPK Q8 times 3 (to check for rise in CPK)

    CPK Isoenzymes (CKI, CPKI, CKMB)
      Differentiates between heart and other muscle.
      May not be as high as you expect because there isn’t enough circulation to the
       area to pick up the enzymes.
      A patient receiving thrombolytics may have very high CPK.

    LDH (Lactic Dehydrogenase)
      Rises about 48-72 hours after CPKs. (2-3 days)
      Not beneficial in early MIs

    Troponin:
      Rises in 3-6 hours
      Peaks in 14-24 hours
      Returns to normal in 10-15 days
      Cardiac sensitive and specific in late MIs

    EKG
      ST elevation and Q wave indicate area of MI

 Treatment Goals
   Relieve distress (pain)
   Limit size of infarct—keep necrotic areas as small as possible
   Decrease cardiac work with meds to allow heart to rest
   Prevent complications—CHF, arrhythmias, etc.

 Thrombolytic Therapy
   ***Understand the difference between thrombolytic therapy and heparin
   Thrombolytics: Enzymes that dissolve clots. Heparin: keeps clots from getting
     larger and allows body’s own mechanisms to dissolve the clot.
   Contraindicated in patients with ulcers, surgery within past month, female on
     period, recent CVA, Systolic BP >180, history of bleeding for any reason.
   No “reverser”/antidote for Thrombolytics. Protamine sulfate is antidote for
   Must be given as soon as possible after onset of chest pain (within 6 hours,
     preferably 4 hours). If given later, med will dissolve clot, but no use as tissue is
     dead. Purpose of Thrombolytic therapy is to prevent more muscle damage.
Myocardial Infarction; Congestive Heart Failure                                        3
Lecture Date 03-03-03                                                                 LJ
    If thrombolytics are given after 8 hours, the area that’s been without blood supply
     is most likely necrotic already.

    Most common thrombolytics:
      Streptokinase:
        Actually a strep bacteria, so pt may develop fever, sore throat, rash,
           aching—can actually give the patient a strep infection. Nice. 
        Don’t use it much anymore for these reasons.
      TPA (Tissue Plasminogen Activator)
        $2,500/dose, but only one does is needed.
        No “flu” symptoms
        Controversial b/c of cost.
      Urokinase
        Rarely used for MIs, but still available.
      Retavase: most commonly used now!
        Given in continuous IV infusion bag over 12 hours
        Lyses clot

    Complications of thrombolytic therapy:
      Bleeding—most common

                                MI Patient in CCU
 Equipment
   Cardiac Monitor
   IVs—at least two.
   Depending on severity:
      Ventilator
      Swan-Ganz
      Arterial Line
      Intra-aortic balloon pump
      Foley
 Nursing Care:
  1. Continuous cardiac monitoring in CCU. Treat arrhythmias.
        a. Ventricular: Lidocaine or amnioterone: PVC and Vtach
        b. Bradycardia: Atropine
        c. Ventricular fibrillation—defibrillate.
  2. Respiratory
        a. Oxygen
        b. Ventilator
        c. Lung sounds—crackles, edema b/c of fluid secondary to CHF
  3. Heart Sounds
        a. Murmur? Is there a murmur developing? If the vessel affected is feeding a
            valve, then the valve can be damaged. Murmur is the 1st sign of damaged
Myocardial Infarction; Congestive Heart Failure                                     4
Lecture Date 03-03-03                                                              LJ
           b. S3 or S4?
   4. Urine Output:
           a. Low—decreased CO = decreased kidney output.
   5. Abdomen:
           a. Decreased bowel tones b/c of decreased CO and intestinal perfusion.
   6. Pulses:
           a. Weak? Thready?
   7. Neuro
           a. Alert? Oriented? Cooperative?
           b. Able to follow commands?
   8. Edema:
           a. Especially pedal edema = CHF sign
   9. Chest pain: New pain could be:
           a. New occlusion of vessel (e.g. secondary to stint placement)
           b. Pericarditis—inflammation of pericardial sac
           c. Treatment: Morphine 2-4 mg IV; Nitroglycerine IV or Sublingual—dilates
               blood vessels so more oxygen and blood can get to painful area.
   10. Monitor Lab values:
           a. K+ Increased or decreased can cause arrhythmias
           b. Magnesium = arrhythmias
           c. CPK (CKI) cardiac enzymes
           d. PT/PTT especially if pt is on heparin or thrombolytics
   11. Bedrest or bathroom privileges
   12. frequent VS. Low BP may indicate decreased CO
   13. Be prepared for Code Blue
   14. Diet—may be on clear liquids 1st day. 2 gm sodium (low sodium and low fat
   15. Maintain a therapeutic environment
   16. Restrict visitors first few days
   17. Denial of MI is common. Anxiety and mood changes reflect coping mechanisms
   18. Explain all procedures and tests.

               Common Medications Used in the Treatment of MIs
   1. ASA (aspirin therapy) decreases platelet aggregation. Does not affect clotting
      mechanism, but makes the platelets “slippery so that they slide through.”
   2. Nitroglycerine (Tridil)continuous IV drip
   3. Heparincontinuous IV drip—Does not dissolve clots. Dose individual to
      maintain PTT at twice the normal.
   4. Dopamine—continuous IV drip
   5. Anti-arrhythmic IV (To tx arrhythmias)
   6. Oral vasodilator
   7. Stool softenerto decrease straining with stools and decrease Valsava maneuver.
      (Valsava stimulation can cause client to “pass out.”)
   8. Diuretic
Myocardial Infarction; Congestive Heart Failure                                           5
Lecture Date 03-03-03                                                                    LJ
   9. Lovenox: Not used in acute phase b/c it’s SubQ. Use when on the floor and

                      New National guidelines for patients with MIs:

                          1.  Aspirin
                          2.  Beta blocker
                          3.  ACE inhibitor
                          4.  If client is a smoker, must address that issue with client and
                              document in the chart.
**Significant research suggests that survival rate post-MI and reinfarcts are reduced with
this treatment. These guidelines should hopefully be in effect within 18 months in all US

                                Complications of MIs
1. Heart failureoccurs in 2/3 of all patients
   2. Hypoxemiamontior O2 sats and administer O2.
   3. HypotensionDetermine cause and treat. (Hypovolemia, Nitroglycerin, large
   4. Cardiogenic ShockHeart cannot pump enough blood to adequately provide O2
      to organs and tissues. Pt. goes into shock state where the organs in body do nto
      get enough O2/blood supply.

                               Congestive Heart Failure

 Definition: Failure of the heart to function as a pump so that it cannot deliver an
  adequate supply of oxygenated blood to the tissues.

 Causes:
   MI
   Valve disease (valve stuck open or closed)
   Cardiomyopathy
   Fluid volume overload
   Hypertension—Higher bp = harder work for the Left ventricle to adequately
     perfuse the body.

 Terminology
   Preload: The force distending the relaxed myocardial fibers. Filling pressure.
     Blood coming to the right heart—pressure before contraction.
   After-load: The force necessary to initiate output to overcome the resistance in the
     vascular system. Amount of resistance after contraction.
   Stroke volume: The amount of blood ejected by the left ventricle during systole.
Myocardial Infarction; Congestive Heart Failure                                       6
Lecture Date 03-03-03                                                                LJ
 Compensatory Mecanisms: When the tissues stop receiving adequate perfusion, the
  body makes some adjustments to try to increase perfusion. These are called
  compensatory mechanisms:
   Increase heart rate
   Starling’s law: Stretching and extension of myocardial muscle fibers. At first this
     increases force of contractions but only works up to a point. Rubber band
     analogy: Professor’s brother’s used to snap her with rubber bands. After repeated
     stretching of rubber band, the rubber band would lose it’s stretch. Same with this
     compensatory mechanism of the heart. Will end up with heart muscle
     overextension and decreased ability of the muscle to contract back down to
     original size.
   Increase stroke volume
   Increase oxygen extraction: Tissues can increase oxygen extraction. Take out
     more O2 when blood supply gets there.

 Left Heart Failure:
   Decreased cardiac output to the system
   Blood backs up into the lungs
   S&S:
      Dyspnea,
      Rales
      Tachycardia
      Paroxysmal nocturnal dyspnea—PND=cannot breathe laying down. Fluid
        redistributes when supine.
      S3 gallop
      SOB

    Acute Pulmonary Edema: Severe Stage of L ventricle failure. Life threatening
     manifestation of acute left vent failure. There is rapid movement of plasma fluid
     into interstitial spaces and alveoli. S&S:
      Extreme dyspnea: SOB
      Cyanosis
      Tachypnea—heavy, fast breathing
      Restlessness
      Anxiety
      Sense of suffocation
      Pale skin
      Thready pulse: “Thin” pulse. Can feel the pulse, but it feels thin.
      Sweating
      Labored respirations
      Pink frothy sputum—looks like pink, foamy bubble suds
      May hear rales up to apices of lungs.

 Right Heart Failure:
Myocardial Infarction; Congestive Heart Failure                                          7
Lecture Date 03-03-03                                                                   LJ
    Right heart unable to pump blood sufficiently to the lungs
    Blood backs up into the system
    S&S
      Enlarged tender liver
      Edema of lower extremities
      Jugular vein distension
      Ascites: fluid collection into abdomen
      Cyanosis—not usually seen unless very severe R sided failure.

 Treatment of Heart Failure: depends on what stage of failure the patient is in.
   Rest:
      Sedate if necessary
      Decreases heart rate and work load
      Elevate HOB
   Rhythm
      Evaluate and treat arrhythmias: PVCs, PACs (premature atrial contractions),
      PVC’s and PAC’s usually improve as congestion subsides.
   Diuretics:
      Lasix: 20-40 mg IV. Can be up to 80 mg Q2 hours!
      The BIG treatment!
      Acts as a potent venodilator before the onset of diuresis and thus decreases
        venous return in early treatment.
      Pulls off potassium. Monitor K+ and supplement prn.
   Digitalis/Digoxin:
      Increases myocardial contractile force: helps heart pump stronger
      Increases renal blood flow
      Slows heart rate—if tachy, will slow down heart rate.
      Note: Dig toxicity: Must watch for and assess for S&S of digoxin toxicity!

**Extra Notes on Digoxin:
 Administration:
    Ascultate apical pulse checked for one full minute immediately before giving
    Hold if apical pulse is <60 in adults or <90-100 in children
    Monitor serum digoxin level and hold if level is > 2.0 ng/dL
    Draw serum digoxin levels 6-8 hours after dose or just before administering next
    Digoxin Toxicity S&S:
        N/V
        Visual disturbances: especially “yellow or blue tints to lights”
        Bradycardia
    Assess for hypokalemia. If K+ < 3.5 cannot give Digoxin. If you give digoxin in
       a hypokalemic state, you will induce dig toxicity. If on Lasix, you will most likely
       give K+ supplements as lasix is a potassium depleting diuretic.
Myocardial Infarction; Congestive Heart Failure                                     8
Lecture Date 03-03-03                                                              LJ
    Treatment of digtoxicity:
      Digibind: Increases renal excretion of Digoxin—usually given with 10-15
        ng/ml (severe toxicity). Life threatening arrhythmias, hypotension or LOC.

    Vasodilators:
      Act on arteries or veins but most have mixed effect
      Nitroprusside (Nipride)—relaxes veins and arteries’ resistance
      Apresoline—dilates arteries and decreases peripheral vascular resistance
      Nitrates—primarily vein dilators with lesser effects on arteries. Watch for
        headache and hypotension.
    ACE Inhibitors:
      Effective in patients with advanced failure
      Decreases afterload, increases cardiac output
      Dobutaminemcg/kg/min continuous infusion. Causes heart muscle to pump
        with more force. Stronger than digoxin.

                                    Nursing Care
 Cardiac Monitoring
   Arrhythmias                                    Pulses
                                                     Weak/thready—heart failure
 Respiratory                                        Bounding—fluid overload/CHF
   Rales/crackles
   Cyanosis                                       Neuro—confusion secondary to
   SOB                                             inadequate perfusion
   Ventilator
                                                   Edema
 Heart Sounds
   S3 Gallop—indication of fluid
     overload                                      Lab Values
                                                     CPK initially to rule out MI
 Urine Output                                       K+ always monitor—especially
   Decrease = not enough cardiac                      if on Lasix, Digoxin
     perfusion or decreased CO
                                                   Bedrest
 Abdomen
   Ascites                                        Elevate HOB
   Decreased bowel tones

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